Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Psychosis only rarely occurs in patients with untreated Parkinson's disease. Much more commonly, psychosis is induced by drug therapy for Parkinson's disease and is the strongest known risk factor for nursing home placement. Delusions are less frequent than hallucinations, but are more concerning as they are often paranoid in nature. Treatment begins with a search for correctable infectious, toxic, and metabolic aetiologies. If symptoms persist, anti-Parkinson's disease medications are slowly reduced. However, withdrawal of these drugs usually worsens parkinsonism and is often not tolerated. Certain atypical antipsychotics can be used to treat psychosis without compromising motor function. The choice of atypical antipsychotic is largely based on ease of use and adverse effect profile as most have comparable efficacy in improving psychosis. Currently, there are five marketed atypical drugs - clozapine, risperidone, olanzapine, quetiapine and ziprasidone. Ziprasidone is the only agent whose adverse effect profile has not been reported in Parkinson's disease. The most common adverse effects of clozapine in Parkinson's disease are sedation, orthostatic hypotension and sialorrhoea. Sedation is generally helpful since these patients are frequently awake at night and tend to have worse behavioural problems then. Clozapine does not induce deterioration of motor function, but it has the potential to cause agranulocytosis, which is idiosyncratic and not dose-related. In risperidone-treated Parkinson's disease patients, reported adverse effects include somnolence, sialorrhoea, dizziness, palpitations, constipation, delirium, fatigue, leg cramps, depression, urinary incontinence and hypotension. Although in some Parkinson's disease studies, risperidone has been well tolerated, others have shown that many patients are unable to tolerate the drug due to deterioration of motor function. While an initial study of olanzapine in Parkinson's disease psychosis showed the drug to be effective without deterioration of motor function, succeeding reports demonstrated a deleterious effect of the drug on motor functioning. The most common adverse effects of quetiapine in Parkinson's disease patients are sedation and orthostatic hypotension. There is a lack of double-blind trials; however, cumulative reports involving >200 Parkinson's disease patients strongly suggest that quetiapine is well tolerated and effective. Unlike clozapine, it does not improve tremor and may induce mild deterioration of motor function. Recently, cholinesterase inhibitors have been reported to alleviate psychosis in Parkinson's disease. Although ondansetron, an antiemetic with antiserotonergic properties, has been reported to relieve psychosis in Parkinson's disease, its prohibitive cost has prevented further study in this population. Electroconvulsive treatment is generally reserved for the patient with psychotic depression who is unable to tolerate any pharmacological therapy.
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PMID:Treatment of psychosis in Parkinson's disease: safety considerations. 1281 32

Thalidomide, an agent with antiangiogenic and immunomodulatory properties, is therapeutically effective in multiple myeloma, leprosy, and autoimmune diseases. The most common clinical toxicities of thalidomide are constipation, neuropathy, fatigue, sedation, rash, tremor, and edema. We here describe for the first time a patient who developed leukocytoclastic vasculitis during therapy with thalidomide. Of the 260 patients treated with thalidomide in our institution, this is the first patient who developed autoimmune disease. We conclude that patients with malignant disorders who are treated with thalidomide should be carefully monitored for the development of autoimmune disorders. Whether autoimmune phenomena also occur during treatment with new drugs such as PS-341 or potent immunomodulatory agents remains to be evaluated.
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PMID:Development of leukocytoclastic vasculitis in a patient with multiple myeloma during treatment with thalidomide. 1462 89

Thalidomide has anti-angiogenic and immunomodulatory activity, exhibiting antitumour effects in patients with multiple myeloma and, more rarely, in several other solid tumours. We evaluated the single-agent antitumour activity and toxicity profile of thalidomide in patients with metastatic malignant melanoma, as well as its plasma pharmacokinetics and pharmacodynamic effects [vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (b-FGF) levels]. A two-stage Gehan method was used with a stopping rule after 14 consecutive non-responding patients. Thalidomide was given orally at a daily dose of 200 mg/day, which was then escalated every 2 weeks by 200 mg/day as tolerated to a maximum of 800 mg/day. Patients were evaluated every 8 weeks for response using the World Health Organization (WHO)-27 criteria. Fourteen patients were enrolled and no objective responses were observed, with one stable disease and one mixed response. The dose-limiting toxicities were constipation, dizziness and somnolence. Other toxicities were oedema, neuropathy, dry skin, dry mouth, tremor and fatigue. The plasma pharmacokinetics of thalidomide were comparable with those of previous studies in normal volunteers and in patients with advanced prostate cancer. Serum levels of b-FGF and VEGF did not change significantly following drug administration. In conclusion, thalidomide showed poor activity, but acceptable toxicity, in patients with metastatic melanoma. Future studies should explore this agent in combination with other biological agents or cytotoxic agents, such as temozolomide.
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PMID:Phase II study of thalidomide in patients with metastatic malignant melanoma. 1557 25

A 74-year-old man became unable to walk two days following the initiation of administration of oral distigmine bromide, 10 mg per day, for his constipation. Neurological examination revealed bradykinesia, rigidity and fine postural tremor without laterality. T2 weighted MRI showed mild front-temporal atrophy and multiple hyperintensities in both deep white matters. His symptoms fully improved one week after discontinuance of distigmine bromide. This is the first case report of distigmine bromide induced Parkinsonism.
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PMID:[Distigmine bromide induced Parkinsonism. A case report]. 1618 Jul 10

The phenotype of 16 members of a family affected by a late-onset, dominant, progressive, motor and autonomic disorder is described. The VAPB (Pro56Ser) mutation was detected in Brazilian families with different phenotypes of motor neuron disorders. In this family, proximal and axial muscle weakness and atrophy, associated with abdominal protrusion, defined the motor phenotype. Death occurred in 10-15 years due to respiratory insufficiency. Tone and tendon reflexes were decreased and a distal tremor was common. Sensation was preserved. Autonomic abnormalities were also present, including choking, chronic intestinal constipation, sexual dysfunction, and sudomotor abnormalities, and on nerve morphology there was involvement of unmyelinated fibers. Electromyography disclosed ongoing denervation and reinnervation. Isolated dysfunction of motor and autonomic neurons is unusual among the spinal muscular atrophies. On this basis, this condition seems to represent a new category of disease.
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PMID:Expanding the phenotypes of the Pro56Ser VAPB mutation: proximal SMA with dysautonomia. 1696 88

Botulinum toxins are an effective treatment modality for a growing number of neurologic conditions. Although there has been varied interest and success in their use, they have been studied for a variety of conditions associated with Parkinson's disease. Conditions reviewed in this paper include hand and jaw tremor, dystonia, blepharospasm and apraxia of eyelid opening, bruxism, camptocormia, freezing of gait, sialorrhea and constipation. We will make comments when applicable on our unique experience with botulinum toxin in these conditions. Other conditions associated with Parkinson's disease, which will not be reviewed here, but may benefit from botulinum toxin treatment include anterocollis (also known as dropped head syndrome), hyperhidrosis, seborrhea and overactive bladder.
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PMID:Botulinum toxin in the treatment of tremors, dystonias, sialorrhea and other symptoms associated with Parkinson's disease. 1756 47

Thalidomide is successfully used in the treatment of multiple myeloma, leprosy and various autoimmune diseases due to its anti-angiogenic, immunomodulatory and anti-inflammatory effects. Thalidomide's most common side effects are constipation, neuropathy, fatigue, sedation, rash, tremor and peripheral edema. We achieved complete response with a 400 mg/day dose thalidomide therapy in a 58-year-old male patient diagnosed with relapsing refractory multiple myeloma. While continuing thalidomide for sustainable response, the therapy was terminated at the ninth month due to development of leukocytoclastic vasculitis. We describe the case and discuss the place of thalidomide in the treatment of multiple myeloma and the rare occurrence of leukocytoclastic vasculitis during thalidomide therapy in multiple myeloma, since only one such case has been reported in the literature thus far.
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PMID:Leukocytoclastic vasculitis due to thalidomide in multiple myeloma. 1770 5

Headache makes one of the most common side effects of frequently pesticide application. This is to be taken care of in rural areas. Headaches have been reported with the use of ivermectin, ivermectin-diethylcarbamazine, organophosphates, and also with the fungicide maneb and copper sulfate, carbofuran, hexonal, dioxin, methomyl and its salts, as well as rare cases of poisoning with the fungicide combination of propineb and cymoxanil. Headache often occurs after long term work with pesticides and/or in laboratories. There are numerous symptoms accompanying headache in pesticide poisoning the most common being elevated body temperature, lassitude, dizziness, irritability, nausea, vomiting, epigastric pain, diarrhea, myalgia, pains in the arms and legs, sleepiness, pains in joints, irritation of eyes/face/skin, sweating. Much less common are respiratory disturbances, tachycardia, tachypnea and other cardiac distur bances, fall of blood pressure, gastrointestinal discomforts, constipation, poor appetite, significant decrease in leukocyte count, anemia, albuminuria, azotemia, fasciculations, miosis, blurred vision, memory disturbances and other neurologic disturbances, postural tremor, signs of cerebral function damage, bradykinesia, etc.
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PMID:[Headache caused by pesticides--a review of the literature]. 1871 90

The objective of this study was to evaluate the efficacy, safety, and tolerability of istradefylline 20 mg once daily versus placebo as an adjunct to levodopa in subjects with Parkinson's disease (PD) who have motor fluctuations. Istradefylline (KW-6002) is an adenosine A(2A) receptor antagonist that in primate models of PD improves motor function without causing or worsening dyskinesia. This 12-week, multicenter, double-blind, placebo-controlled, randomized, Phase 3 study of istradefylline was conducted in subjects experiencing an average daily OFF time of at least 3 hours (116 randomized to istradefylline; 115 to placebo). All were on stable levodopa regimens; 90% were also on stable regimens of other anti-Parkinson's medications. Istradefylline-treated subjects had significant placebo-corrected reductions in daily OFF time from baseline to endpoint: 4.6% (P = 0.03) and 0.7 hours (P = 0.03). For ON time with troublesome dyskinesia, the changes between istradefylline and placebo were not significant. Istradefylline was well tolerated, with 6 (5.2%) istradefylline-treated and 7 (6.1%) placebo-treated subjects withdrawing from the study because of adverse events. Dyskinesia, lightheadedness, tremor, constipation, and weight decrease were reported more often with istradefylline than placebo. We conclude that istradefylline is well tolerated and significantly reduces OFF time as an adjunct to levodopa in PD subjects with motor fluctuations.
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PMID:Study of istradefylline in patients with Parkinson's disease on levodopa with motor fluctuations. 1883 30

Botulinum toxin (BoNT) has been used for over a quarter of century for the treatment of well over 100 different indications. Many of the symptoms for which BoNT has been found to be effective occur in a variety of neurological disorders. One neurodegenerative disorder in which BoNT has been used extensively to treat various symptoms is Parkinson's disease (PD). This review will highlight the following therapeutic applications of BoNT in conditions associated with PD: limb dystonia, blepharospasm and lid apraxia, bruxism, cervical dystonia (anterocollis), camptocormia, hand and jaw tremor, rigidity (painful shoulder), freezing of gait, sialorrhea, dysphagia (achalasia), seborrhea, hyperhidrosis, overactive bladder, and constipation.
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PMID:Disease-oriented approach to botulinum toxin use. 1907 3


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